INTRODUCTION

Novel coronavirus disease 2019 (COVID-19), which is known as coronavirus-induced pneumonia, is a member of the family Coronavirdae named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). In December 2019, this virus developed in Wuhan, a city in the Hubei Province of China, then the World Health Organization (WHO) announced the Public Health Emergency of International Concern (PHEIC) at the end of January 2020. On 11^th March 2020, COVID-19 is considered a pandemic disease that shares about 80% sequence identity with SARS-CoV-1 [1]. Therefore, SARS-CoV-1, SARS-CoV-2, and Middle East respiratory syndrome CoV (MERS-CoV) are known as highly pathogenic human coronavirus infections that cause high mortality and morbidity [2, 3]. Up to date, there are about 577,429,314 confirmed cases of COVID-19 around the world of which 547,241,709 (94.77%) were cured, 6,407,868 (1.11%) were dead and the rest patients were either stable with about 23,779,737 (4.12%) or in critical situation 41,677 (0.01%). In Saudi Arabia, there are approximately 808,419 confirmed cases of coronavirus disease, 792,842 (98.07%) of the Saudi population recovered, while 9,243 (1.14%) of them were dead. Pneumonia appears to be the most common serious manifestation of COVID-19, characterized by fever, dry cough, fatigue, myalgia, dyspnea with acute respiratory distress syndrome (ARDS), and lymphopenia [4-6]. The cellular immune response is a crucial component of the immune defense that can recognize and control intracellular SARS-CoV-2 infection. However, an immunological role for orchestrated acute mortality from patients with SARS-CoV-2 is not yet illustrated. Therefore, the purpose of this review is to deliver an overview of the immune pathogenesis and T-cell response of SARS-CoV-2 infection, as well as, recent clinical diagnosis, treatment, and therapeutic/prophylactic vaccines against COVID-19, hinging on the information of two types of coronavirus; MERS and SARS that may assist in designing the appropriate immune intervention for.

Immune Pathogenesis of SARS-Cov-2 Infection

Immune function is considered a vital defense mechanism against infectious invasive pathogens. To facilitate the recognition of this new infection, the immunological mechanism of SARS-CoV-1 and MERS-CoV need to be addressed, especially changes in peripheral T-cells, their subsets, and B-cells. Coronaviruses classically infect the upper respiratory tract, however, MERS-CoV, SARS-CoV, and SARS-CoV-2 infect the lower respiratory tract and lead to pneumonia, which can be fatal.

Coronavirus is enveloped by single-stranded (ss), positive-sense RNA viruses’ genome (26-32 kb). Two-thirds of the viral RNA open reading frame (ORF1a/b) encodes polyproteins that form the viral replicase transcriptase complex in MERS-CoV, SARS-CoV, and SARS-CoV-2. While, other ORFs on one-third of the genome encode four main structural proteins; spike (S), membrane (M), nucleocapsid (N), envelope (E), and other accessory proteins that do not participate in the replication of the virus [7] (Figure 1). Coronavirus  S-protein presents on the viral surface and this feature determines virus entry into the host cells-surface significantly, as angiotensin-converting enzyme 2 (ACE2) [8]. ACE2 is a receptor that binds to the envelope S glycoprotein of SARS-CoV-1 and SARS-CoV-2 [9, 10], dipeptidyl peptidase 4 (DPP4) for MERS-CoV, and CD209L for SARS-CoV [11]. This type I membrane protein (51), ACE2, are prone to viral infection by expressing on several cell types, such as heart, kidney, blood vessels, gastrointestinal tract, and lung alveolar type II epithelial cells [12]. After attachment to cellular receptor(s), enveloped SARS-CoV-1 requires membrane fusion to enter host cells at the plasma membrane [13]. Subsequently, the genomic RNA of the virus is released into the cytoplasm, then uncoated RNA is translated into two polyproteins, after which the sub-genomic RNA begins to transcript and replicate [7, 14]. As a result, these newly synthesized proteins insert into the endoplasmic reticulum (ER) membrane, and the Golgi apparatus and N are formed. Eventually, the newly formed virion is often seen inside vesicles, then fuses with the plasma membrane to secret it [3] (Figure 2).